Wnt signaling in disease and in development

By R. Nusse. Cell Research, 2005

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The GSK3 hypothesis of Alzheimer's disease (2008, background): “In the absence of Wnt, the signaling pool of b-catenin is maintained at low levels through degradation (Dale 1998; Huelsken and Behrens 2002; Nusse 2005). b-catenin is targeted for ubiquitination by the b-transducin repeat containing protein (bTrCP) and is then degraded by the proteosome. b-catenin…”
Histone lysine methyltransferase Wolf-Hirschhorn syndrome candidate 1 is involved in human carcinogenesis through regulation of the Wnt pathway. (2011, background): “On the contrary, although the dysregulation of WNT signaling in various types of cancer has been implied [45,46], such mutations seem to be rare in a number of cancers including bladder and lung carcinomas [38,47,48].”